Mechanisms of adverse effect of amaranth feeding in the rat.

Abstract

SummaryIn order to clarify the mechanism of the adverse effects of dietary amaranth, trisodium 1-(4-sulfo-l-naphthylazo)-2-naphthyl-3,6 disulfonic acid, the effects of amaranth in vitro and in a jejunum perfusion in vivo on intestinal sucrase were investigated in rats. The inhibitory effect of amaranth in vitro on the sucrase activity was not detected even at the concentration of 1%, whereas the remarkable release of intestinal sucrase from intestine was observed with the jejunum perfusion of Ringer bicarbonate solution (RBS) containing amaranth at the 1% level. On the other hand, the perfusion of RBS containing tris (hydroxymethyl) -aminomethane, a strong inhibitor of intestinal disaccharidase activities, did not produce the release of intestinal alkaline phosphatase. These findings suggest that the toxicity of dietary amaranth is due to the exfo liating or solubilizing effects of amaranth on the brush border membrane of the small intestine. Key Words small intestine, sucrase, perfusion, amaranth, tris (hydroxy methyl) aminomethaneErshoff (1) and Ershoff and Marshall (2) reported that toxicities, significant growth retardation and severe diarrhea of non-ionic surface-active agents added to a highly purified diet were counteracted by the concurrent feeding of dietary fiber. In the previous studies (3-6) we reported that the mechanisms were the exfoliating or solubilizing effects of these detergents in the brush border membrane of the small intestine, and that the dietary fiber prevented these effects. The toxicities of amaranth feeding as well as those of non-ionic surface-active agent feeding were prevented by the concurrent feeding of dietary fiber (7,8). However, the mechanism of the toxicities caused by amaranth feeding remains unclear, although we suggested